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Long non-coding RNA, FOXP4-AS1, acts as a novel biomarker of cancers

  • Liang Yu and Juan Lu EMAIL logo
Published/Copyright: September 12, 2023
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Oncologie
From the journal Oncologie Volume 25 Issue 6

Abstract

Long non-coding RNAs (lncRNAs) are a recently discovered class of non-coding RNAs with a length of more than 200 nucleotides. Dysregulation of lncRNAs has been implicated in the development and progression of various human diseases and has pivotal functions in diverse biological processes, like cell apoptosis, proliferation, migration, and invasion. LncRNAs are increasingly being identified as potential targets for clinical applications based on their functional mechanisms, which are gradually being elucidated. One such disease-related lncRNA is the forkhead box P4-AS1 (FOXP4-AS1), which is abnormally expressed in multiple human diseases, including cancer and non-cancerous diseases. Moreover, FOXP4-AS1’s expression is linked with the clinical characteristics of patients. Mechanistically, FOXP4-AS1 mediates several cellular processes mainly through its target genes. Therefore, FOXP4-AS1 has been extensively investigated for its diagnostic, prognostic, and therapeutic potential. In this review, we discuss the expression patterns, major role, and molecular mechanisms of FOXP4-AS1, along with its association with clinical features and potential applications in clinical settings.

Keywords: FOXP4-AS1; lncRNA; human·diseases; cancer; prognosis

Introduction

With the continuous development of medical technologies and the advancement of research, genomic medical science and its relationship with the causes of human disorders have received growing attention [1], [2], [3], [4], [5], [6]. Given the widespread application of high-throughput RNA sequencing technologies long non-coding RNAs (lncRNAs), a class of non-coding RNAs with a length of more than 200 nucleotides were recently discovered [7], [8], [9], [10], [11]. LncSEA [12] is a platform with the largest number of human lncRNA sets, having comprehensive annotation with information on enrichment analysis and associated upstream regulators and downstream targets of lncRNAs. The powerful lncRNA platform supports researchers to obtain highly specific functions of lncRNAs of interest. Numerous studies have uncovered that lncRNAs perform significant functions in various physiological and pathological processes, including cell cycle, proliferation, differentiation, apoptosis, inflammatory response, and invasion [13], [14], [15], [16], [17]. LncRNAs regulate gene expression and function through interactions with diverse molecules, such as proteins, RNA and DNA [18], [19], [20], [21], [22], [23], [24]. These unique signatures suggest the crucial advantages of lncRNAs for their diagnostic, prognostic, and therapeutic roles in diverse human disorders [25], [26], [27], [28].

One disease-specific lncRNA of interest is the lncRNA forkhead box P4 (FOXP4)-AS1 (FOXP4-AS1), a recently discovered antisense transcript of FOXP4 located on the chromosome 6p21.1. Its size is 96,181 bases. Several studies suggest that FOXP4-AS1 expression is aberrantly regulated in human diseases, including colorectal cancer [29], [30], [31], esophageal cancer [32, 33], nasopharyngeal cancer [34], [35], [36], liver cancer [37], [38], [39], gastric cancer [40], ovarian cancer [41, 42], cervical cancer [43], lymphoma [44], lung cancer [45], bone cancer [46, 47], pancreatic cancer [48], prostate cancer [49], glioma [50], COVID-19 [51, 52], placenta accreta [53], and thyroid cancer [54]. FOXP4-AS1 levels are strongly correlated with patients’ clinical features and prognosis, along with their TNM stage, tumor size, and lymph node metastasis [32, 34, 47]. FOXP4-AS1 participated extensively in disease progression through the regulation of important cellular processes, like cell apoptosis, proliferation, migration, and invasion [29, 32, 33, 35]. Mechanistic studies have provided a deeper insight into FOXP4-AS1’s interactions with its target genes. FOXP4-AS1 exerts its influence on biological processes by directly modulating the expression of downstream target genes [44, 45]. Functioning as a regulatory factor, it interacts with the DNA or RNA sequence of these target genes, thereby exerting an impact on gene transcription and translational processes. This regulatory mechanism alters the functional state of cells, thereby affecting processes such as cellular proliferation, differentiation, and apoptosis. Furthermore, FOXP4-AS1 is regulated by its upstream molecules. Transcription factors, miRNAs, proteins, and other molecules can interact with FOXP4-AS1, thereby controlling its expressional level within the cell [49]. This upstream regulatory mechanism indirectly affects the expression of downstream target genes by modulating the stability, transcription rate, or translational process of FOXP4-AS1. Consequently, these properties render FOXP4-AS1 as a potential clinical biomarker of disease diagnosis, prognosis as well as a therapeutic target [32, 34, 47, 50].

In this review, we focus on the current understanding of FOXP4-AS1 from the aspects of its expression, functions, and regulatory mechanisms, and discuss its promising clinical applications. Furthermore, recent advancements in the field are reviewed, along with future directions to deepen the understanding of FOXP4-AS1 and its implications in human disorders.

FOXP4-AS1’s expression and its roles in human diseases

The aberrant expression of FOXP4-AS1 plays a significant role in the development and progression of various diseases, including colorectal cancer [29], [30], [31], esophageal cancer [32, 33], nasopharyngeal cancer [34], [35], [36], liver cancer [37], [38], [39], gastric cancer [40], ovarian cancer [41, 42], cervical cancer [43], lymphoma [44], lung cancer [45], bone cancer [46, 47], pancreatic cancer [48], prostate cancer [49], glioma [50], COVID-19 [51, 52], placenta accreta [53], and thyroid cancer [54] (Figure 1). Moreover, there exists a strong correlation between the levels of FOXP4-AS1 expression and clinicopathological features, including overall survival (OS), TNM stage, tumor size, and lymph node metastasis (Table 1). The dysregulation of FOXP4-AS1 has been implicated in the pathogenesis of these diseases through various molecular mechanisms.

Figure 1: The dysregulation of FOXP4-AS1 in human cancers.
Figure 1:

The dysregulation of FOXP4-AS1 in human cancers.

Table 1:

LncRNA FOXP4-AS1 expression and clinical characteristics in human diseases.

Disease type Expression Clinical characteristics Refs
Colorectal cancer Upregulated TNM stages, and tumor size [29], [30], [31]
Esophageal cancer Upregulated Lymph node metastasis, TNM stage, OS, and RFS [32, 33]
Nasopharyngeal cancer Upregulated T stage, clinical stage, lymph node metastasis, OS, and PFS [34], [35], [36]
Liver cancer Upregulated Age, AFP, AST, BCLC stage, tumor size, DFS, and OS [37], [38], [39]
Gastric cancer Upregulated DFS [40]
Ovarian cancer Downregulated FIGO stage, clinical stage, grades, lymphatic invasion, OS, DFS, and PFS [41, 42]
Cervical cancer Upregulated – [43]
Lymphoma Upregulated OS, DFS, and clinical stages [44]
Lung cancer Upregulated – [45]
Ewing Sarcoma Upregulated OS, and EFS [46]
Osteosarcoma Upregulated – [47]
Pancreatic cancer Upregulated OS, and mortality rates [48]
Prostate cancer Upregulated OS, and tumor stage [49]
Glioma Upregulated – [50]
Papillary thyroid carcinoma Downregulated TNM stages, extraglandular invasion, and disease-free interval rate [54]

In this section, we provide a comprehensive discussion of the expression patterns of FOXP4-AS1, its association with clinical factors, and its main major functions in several human disorders.

The abnormal expression of FOXP4-AS1 was observed in colorectal cancer, esophageal cancer, nasopharyngeal cancer, liver cancer, gastric cancer, ovarian cancer, cervical cancer, lymphoma, lung cancer, bone cancer, pancreatic cancer, prostate cancer, and thyroid cancer.

Colorectal cancer

Previous studies demonstrated the high expression of FOXP4-AS1 in colorectal cancer cells, HT29, SW620, SW480, LOVO, DLD1, and HCT116 and tissues [29], [30], [31]. High levels of FOXP4-AS1 are positively associated with worse TNM stages and larger tumor size. Moreover, FOXP4-AS1 promotes cancer by increasing tumor cell proliferation, migration, and invasion and suppressing apoptosis, as evidenced in DLD1, HCT116, and HT29 cells. Moreover, FOXP4-AS1 enhances tumor xenograft growth. The above evidence suggests that FOXP4-AS1 plays a crucial role in the progression and aggressiveness of colorectal cancer. Further understanding of its molecular mechanisms may yield potential therapeutic targets and prognostic indicators for this disease.

Esophageal cancer

FOXP4-AS1 is upregulated in esophageal squamous cell carcinoma (ESCC) tissues and Eca109, TE1, TE13, YES-2, KYSE150, EC9706, KYSE410, and KYSE450 cells [32, 33]. Its expression level is positively correlated with the TNM stage of the disease, lymph node metastasis, OS, and recurrence-free survival (RFS). Additionally, FOXP4-AS1 enhances the proliferation, migration, and invasion abilities of YES-2, KYSE450, and KYSE150 cells, thus promoting the progression of ESCC. These findings suggest that FOXP4-AS1 plays a significant role in the development and aggressiveness of ESCC. Further exploration of its underlying mechanisms may yield potential therapeutic targets and prognostic indicators for ESCC.

Nasopharyngeal cancer

In nasopharyngeal carcinoma, upregulated FOXP4-AS1 expression has been observed in the serum and cell lines including CNE1, HONE1, C666-1, and CNE2 [34], [35], [36]. The relationship between FOXP4-AS1 levels and various clinical features of patients, such as the T stage, clinical stage, lymph node metastasis, OS, and progression-free survival (PFS), has also been investigated. Additionally, the overexpression of FOXP4-AS1 promotes cancer development by enhancing CNE1 cell proliferation, apoptosis, metastasis, and epithelial-mesenchymal transition (EMT). These findings suggest that FOXP4-AS1 may play a critical role in the pathogenesis of nasopharyngeal cancer.

Liver cancer

FOXP4-AS1 is upregulated in various hepatocellular carcinoma (HCC) cell lines, including MHCC97H, HepG2, Hep3B, Huh7, LM3, and SMMC7721, as well as in HCC tissues [37], [38], [39]. FOXP4-AS1’s overexpression is associated with several clinical characteristics of HCC patients, such as age, serum aspartate aminotransferase (AST), alpha-fetoprotein (AFP), BCLC stage, tumor size, disease-free survival (DFS), and OS. Furthermore, FOXP4-AS1 aggravates HCC progression and is involved in promoting cell proliferation, invasion, and migration of Hep3B, Huh7, SMMC-7721, and LM3 cells. It can stimulate angiogenesis in human umbilical vein endothelial cells (HUVECs) and increase the size of HCC tumors in mice. These findings highlight the significance of FOXP4-AS1 in the development and aggressiveness of HCC and suggest its potential as a therapeutic target and prognostic marker for this deadly disease.

Gastric cancer

Elevated FOXP4-AS1 levels have been observed in the gastric cancer cells, AGS, NCI-N87, and MKN-45 and tissues, and its overexpression is associated with poorer DFS [40]. These results underscore the potential oncogenic role of FOXP4-AS1 in gastric cancer and suggest its promising role as a therapeutic target.

Ovarian cancer

Recent studies have revealed that the downregulation of FOXP4-AS1 in ovarian cancer restrains EMT and even mediates immune cell infiltration and inflammatory responses [41, 42]. High FOXP4-AS1 expression correlates positively with favorable International Federation of Gynecology and Obstetrics (FIGO) stage, clinical stage, grades, lymphatic invasion, OS, DFS, and PFS of patients with ovarian cancer.

Other diseases

FOXP4-AS1 is differentially upregulated in cervical cancer and accelerates the malignant behavior of Caski and C33A cells, thus worsening the progression of cervical cancer [43]. Similarly, FOXP4-AS1 accelerates mantle cell lymphoma development by elevating the proliferative and metastatic abilities of the JVM-2 and Z138 cells [44]. High FOXP4-AS1 level correlates with poor OS, DFS, and clinical stages in patients with lymphoma. FOXP4-AS1 is upregulated in non-small cell lung cancer (NSCLC) A549, Calu‐1, and H1299 cells as well as tissues [45]. FOXP4-AS1 was proposed as a cancer‐promoting regulator which enhances the proliferative function of A549 and Calu‐1 cells and xenograft tumor growth in nude mice. As for bone cancer, FOXP4-AS1 was found to be remarkably upregulated in Ewing Sarcoma SK-N-MC, and A673 cell lines, and led to worse OS and event-free survival rates (EFS) in these patients. FOXP4-AS1 resulted in aggressive Ewing Sarcoma by enhancing cell invasion, proliferation, and migration [46]. FOXP4-AS1 was also upregulated in HOS, A673, SK-N-MC, MG63, Saos2, and U2OS osteosarcoma cells. FOXP4-AS1 accelerated the proliferation, migration and inhibited the apoptosis of A673, SK-N-MC, MG63, and U2OS cells, thereby promoting tumor formation [47]. Moreover, high FOXP4‐AS1 expression in pancreatic cancer strongly correlates with poor prognosis and was found to increase cancer‐related mortality rates in these patients [48]. FOXP4‐AS1 is highly expressed in prostate cancer PC-3, DU145, VCaP, and LNCaP cells and tissues [49]. High FOXP4‐AS1 levels reflect poorer OS and tumor stage in patients with prostate cancer. In vivo animal studies and in vitro cytological experiments demonstrate that FOXP4-AS1 exerts a crucial function on prostate cancer progression by facilitating cell proliferation and repressing cell apoptosis. FOXP4-AS1 is downregulated in both papillary thyroid cancer (PTC) tissues and cell lines (K1, BCPAP, and TPC-1). Higher expression levels of FOXP4-AS1 are associated with more favorable patient outcomes, lower TNM stages, and reduced extra glandular invasion. Mechanistically, FOXP4-AS1 exerts its inhibitory effects on PTC progression by negatively regulating FOXP4 expression and suppressing the activity of the Akt signaling pathway [54].

Apart from its involvement in cancer, FOXP4-AS1 functions in other human disorders. Notably, a Japanese genome-wide association study (GWAS) reported that FOXP4-AS1 is related to the initiation and severity of the COVID-19 disease [51]. A COVID-19 Host Genetics Initiative (HGI) analysis also suggested that the common variants of FOXP4-AS1 may regulate patients’ adaptive immunity, and therefore, are closely associated with COVID-19 disease severity [52].

Mechanisms of FOXP4-AS1 action in human disorders

Numerous studies have provided evidence for the role of FOXP4-AS1 dysregulation in driving the progression of various human diseases by mediating diverse cellular processes, including proliferation, apoptosis, migration, and invasion [35], [36], [37]. These findings highlight the diverse and multifaceted roles of FOXP4-AS1 in human diseases, underscoring its potential as a diagnostic marker, prognostic predictor, and therapeutic target. Therefore, in this section, we briefly introduce the predominant mechanisms underlying the biological functions of FOXP4-AS1 in several human disorders.

The irregular regulation of cell proliferation and apoptosis often results in uncontrollable cell growth and eventual cancer formation [55], [56], [57], [58]. Aberrant cell migration and invasion drive tissue metastasis, accounting for over 90 % of cancer-associated deaths [59], [60], [61], [62], [63]. Therefore, an in-depth understanding of the mechanisms of these essential biological processes is becoming an increasingly attractive approach for the development of new treatment types. FOXP4-AS1 has been implicated in the development and progression of different types of human disorders, such as CRC, esophageal cancer, nasopharyngeal cancer, liver cancer, gastric cancer, pancreatic cancer, ovarian cancer, cervical cancer, prostate cancer, lung cancer, lymphoma, Ewing Sarcoma, osteosarcoma, glioma, and even COVID-19 (Table 2). Recent studies have shown that FOXP4-AS1 is activated by ATF3, leading to the acceleration of malignant processes in colorectal cancer HCT116 cells. This occurs through the interaction of FOXP4-AS1 with miR-423-5p, resulting in the upregulation of NACC1 expression [29]. Additionally, FOXP4-AS1 promotes cell migration, invasion, and proliferation in esophageal cancer cell lines, KYSE150 and KYSE450, which is mediated by the MLL2/FOXP4 axis by enhancing β-catenin expression. FOXP4-AS1 also interacts with IGF2BP2 proteins and miRNA-3184-5p to regulate FOXP4 levels in esophageal cancer cells (Figure 2) [32, 33]. In nasopharyngeal cancer, FOXP4-AS1 interferes with miR-423-5p expression, leading to elevated STMN1 levels and the positive regulation of proliferative ability of CNE1 cells [35]. FOXP4-AS1 facilitates metastasis and EMT in C666-1 cells through the miR-136-5p/MAPK1 axis [36]. FOXP4-AS1 increases H3K27me3 levels through the recruitment of EZH2, thus inhibiting ZC3H12D expression in HCC SMMC-7721 and LM3 cells and promoting cell proliferation, invasion, and migration [37]. In cervical cancer, upregulated FOXP4-AS1 boosts malignant transformation processes in C33A and Caski cells by binding with miR-136-5p to enhance CBX4 expression [43]. FOXP4-AS1 interacts with miR-423-5p to upregulate NACC1, thereby strengthening the proliferation, migration, and invasion of mantle cell lymphoma JVM-2 and Z138 cells [44]. The proliferative process of NSCLC A549 and Calu‐1 cells is also enhanced by FOXP4-AS1 through its combination with miR-3184-5p to promote EIF5A expression [45]. Moreover, FOXP4-AS1 increases TMPO levels by binding to miR-298 and enhances the progression of cell proliferation, migration, and invasion in Ewing Sarcoma SK-N-MC and A673 cells [46]. Furthermore, FOXP4-AS1 combines with LSD1 and EZH2 to weaken the levels of LATS1, in turn facilitating the proliferation and migration of OS MG63 and U2OS cells [47]. In prostate cancer, after the activation of FOXP4-AS1 by PAX5, FOXP4-AS1 sponges with miR-3184-5p and increases the FOXP4 level, thus enhancing the proliferative ability of PC-3 cells [49]. These findings suggest that FOXP4-AS1 plays a significant role in various cancers, contributing to the regulation of cell proliferation, migration, invasion, and malignant transformation processes.

Table 2:

LncRNA FOXP4-AS1 roles and regulatory mechanisms in human cancers.

Disease type Role Cell lines Functions Related mechanisms Refs
Colorectal cancer Tumor promoter HT29, SW620, SW480, LOVO, DLD1, and HCT116 Cell proliferation, apoptosis, migration, and invasion ATF3, miR-423-5p, and NACC1 [29], [30], [31]
esophageal cancer Tumor promoter Eca109, TE1, TE13, YES-2, KYSE150, EC9706, KYSE410, and KYSE450 Cell proliferation, migration, and invasion MLL2, FOXP4, β-catenin, YY1, IGF2BP2, and miR-3184-5p [32, 33]
Nasopharyngeal cancer Tumor promoter CNE1, HONE1, C666-1, and CNE2 Cell proliferation, and apoptosis miR-423-5p, and STMN1 [34], [35], [36]
Liver cancer Tumor promoter MHCC97H, HepG2, Hep3B, Huh7, LM3, and SMMC7721 Cell proliferation, migration, and invasion H3K27me3, EZH2, and ZC3H12D [37], [38], [39]
Gastric cancer Tumor promoter MKN45, NCIN87, and AGS – – [40]
Ovarian cancer Tumor suppressor – Inflammatory response – [41, 42]
Cervical cancer Tumor promoter Caski, and C33A Cell proliferation, migration, and invasion miR-136-5p, and CBX4 [43]
Lymphoma Tumor promoter JVM-2, and Z138 Cell proliferation, migration, and invasion miR-423-5p, and NACC1 [44]
Lung cancer Tumor promoter A549, Calu‐1, and H1299 Cell proliferation miR-3184-5p, and EIF5A [45]
Ewing sarcoma Tumor promoter A673, and SK-N-MC Cell proliferation, migration, and invasion miR-298, and TMPO [46]
Osteosarcoma Tumor promoter A673, SK-N-MC, HOS, Saos2, MG63, and U2OS Cell proliferation, apoptosis, migration, and invasion LATS1, LSD1, and EZH2 [47]
Pancreatic cancer Tumor promoter – – – [48]
Prostate cancer Tumor promoter PC-3, DU145, VCaP, and LNCaP Cell proliferation, and apoptosis PAX5, miR-3184-5p, and FOXP4 [49]
Glioma Tumor promoter – Drug resistance – [50]
Papillary thyroid carcinoma Tumor suppressor K1, BCPAP, and TPC-1 Cell proliferation, apoptosis, and migration FOXP4, and Akt [54]
Figure 2: FOXP4-AS1 enhanced cell proliferation, migration, and invasion in esophageal cancer.
Figure 2:

FOXP4-AS1 enhanced cell proliferation, migration, and invasion in esophageal cancer.

In YES-2 and KYSE150 cells, FOXP4-AS1 combined with MLL2 to upregulate the FOXP4 level and further activated β-catenin expression. In KYSE150 and KYSE450 cells, FOXP4-AS1 interacted with IGF2BP2 protein or miR-3184-5p to enhance FOXP4 expression. Meanwhile, YY1 also elevated the transcription of FOXP4-AS1 and FOXP4.

Clinical application prospects of FOXP4-AS1 in human disease intervention

Although many treatment options have been explored and applied in clinical practice, the global disease burden continues to be heavy, especially that of cancers [64], [65], [66], [67], [68]. Therefore, accurate diagnosis and timely treatment are vital for clinical management and optimizing patient prognosis [69], [70], [71], [72], [73].

Recently, there has been growing interest in the clinical application of FOXP4-AS1 owing to its potential for understanding and managing various diseases. FOXP4-AS1 exhibit differential expression levels in different types of diseases, indicating its involvement in disease mechanisms. FOXP4-AS1 levels are strongly correlated with patients’ clinical characteristics and prognoses. Therefore, FOXP4-AS1 levels have potential diagnostic and prognostic roles in indicating disease progression. To assess the diagnostic accuracy of FOXP4-AS1, researchers frequently employ receiver operating characteristic (ROC) curve analysis. This analysis has confirmed the high diagnostic value of FOXP4-AS1 in distinguishing disease tissues from normal tissues. For example, FOXP4-AS1 possesses a high diagnostic value with an area under the curve (AUC) reaching up to 0.8679 for differentiating ESCC from normal specimens [32]. FOXP4-AS1 expression in nasopharyngeal cancer serum samples has a powerful diagnostic value with an AUC of 0.7974 [34]. In OS, an AUC of 0.851 also suggests the strong diagnostic performance of FOXP4-AS1 [47]. The Kaplan-Meier method also reveals the remarkable association between FOXP4-AS1 expression levels and patients’ clinical features and prognosis across diseases. All of the above results reflect the robust prognostic capability of FOXP4-AS1 in diverse human disorders, such as CRC [30], esophageal cancer [32], nasopharyngeal cancer [34], liver cancer [37], [38], [39], gastric cancer [40], ovarian cancer [41], lymphoma [44], Ewing Sarcoma [46], OS [47], pancreatic cancer [48], and glioma [50]. Furthermore, FOXP4-AS1’s dysregulation has been shown to play a role in modulating crucial biological processes and disease progression by interacting with specific molecules. This discovery opens up possibilities for targeted interventions aimed at manipulating FOXP4-AS1’s expression for therapeutic purposes. Additionally, research has highlighted that FOXP4-AS1 expression can predict the sensitivity of glioma patients to temozolomide treatment, offering potential benefits for personalized medicine [50]. Therefore, FOXP4-AS1 has promising clinical applications in disease diagnosis, prognosis, and potentially even in treatment strategies. The differential expression of FOXP4-AS1 in diseases, its ability to distinguish disease tissues, its correlation with clinical characteristics, and its involvement in disease mechanisms render it an attractive target for further research and development in the field of precision medicine.

In summary, FOXP4-AS1 acts as a disease-related lncRNA and is dysregulated in multiple human diseases, including CRC, esophageal cancer, nasopharyngeal cancer, liver cancer, gastric cancer, ovarian cancer, cervical cancer, lymphoma, lung cancer, bone cancer, pancreatic cancer, prostate cancer, COVID-19, and placenta accreta. Additionally, FOXP4-AS1 levels are closely linked to patient clinical characteristics and prognosis, including age, TNM stage, tumor size, lymph node metastasis, OS, DFS, and RFS. Moreover, FOXP4-AS1 interacts with various target genes, leading to the modulation of crucial cellular processes, like cell invasion, proliferation, migration, apoptosis, and drug sensitivity, all of which suggest the significant role of FOXP4-AS1 in disease progression and treatment response. Given its extensive role and association with human diseases, FOXP4-AS1 is a promising clinical tool for disease diagnosis, prognosis, and designing novel treatment strategies. While the current understanding of FOXP4-AS1 roles is in the initial phase, further in-depth experimental studies and clinical trials are needed to elucidate the underlying biological mechanisms and validate their clinical utility. Looking ahead, future research on FOXP4-AS1 should focus on exploring its specific molecular interactions and downstream signaling pathways. Furthermore, large-scale clinical studies involving diverse patient populations are expected to provide insights into the diagnostic and prognostic value of FOXP4-AS1.

Corresponding author: Juan Lu, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, National Medical Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China, E-mail: .

Funding source: The National Nature Science Foundation of China

Award Identifier / Grant number: U20A20343 and 82200673

  1. Research ethics: The local Institutional Review Board deemed the study exempt from review.

  2. Informed consent: Informed consent was obtained from all individuals included in this study.

  3. Author contributions: All authors have accepted responsibility for the entire content of this manuscript and approved its submission.

  4. Competing interests: Authors state no conflict of interest.

  5. Research funding: This study was funded by the National Nature Science Foundation of China (82200673).

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Received: 2023-07-22
Accepted: 2023-08-21
Published Online: 2023-09-12

© 2023 the author(s), published by De Gruyter, Berlin/Boston

This work is licensed under the Creative Commons Attribution 4.0 International License.

Articles in the same Issue

  1. Frontmatter
  2. Review Articles
  3. Mitochondrial thermogenesis in cancer cells
  4. Application of indocyanine green in the management of oral cancer: a literature review
  5. Long non-coding RNA, FOXP4-AS1, acts as a novel biomarker of cancers
  6. The role of synthetic peptides derived from bovine lactoferricin against breast cancer cell lines: a mini-review
  7. Single cell RNA sequencing – a valuable tool for cancer immunotherapy: a mini review
  8. Research Articles
  9. Global patterns and temporal trends in ovarian cancer morbidity, mortality, and burden from 1990 to 2019
  10. The association between NRF2 transcriptional gene dysregulation and IDH mutation in Grade 4 astrocytoma
  11. More than just a KRAS inhibitor: DCAI abrogates the self-renewal of pancreatic cancer stem cells in vitro
  12. DUSP1 promotes pancreatic cancer cell proliferation and invasion by upregulating nephronectin expression
  13. IMMT promotes hepatocellular carcinoma formation via PI3K/AKT/mTOR pathway
  14. MiR-100-5p transfected MSCs-derived exosomes can suppress NSCLC progression via PI3K-AKT-mTOR
  15. Inhibitory function of CDK12i combined with WEE1i on castration-resistant prostate cancer cells in vitro and in vivo
  16. Prognostic potential of m7G-associated lncRNA signature in predicting bladder cancer response to immunotherapy and chemotherapy
  17. Case Reports
  18. A rare FBXO25–SEPT14 fusion in a patient with chronic myeloid leukemia treatment to tyrosine kinase inhibitors: a case report
  19. Stage I duodenal adenocarcinoma cured by a short treatment cycle of pembrolizumab: a case report
  20. Rapid Communication
  21. ROMO1 – a potential immunohistochemical prognostic marker for cancer development
  22. Article Commentary
  23. A commentary: Role of MTA1: a novel modulator reprogramming mitochondrial glucose metabolism
https://doi.org/10.1515/oncologie-2023-0295
Keywords for this article
FOXP4-AS1; lncRNA; human·diseases; cancer; prognosis
Creative Commons
BY 4.0

Articles in the same Issue

  1. Frontmatter
  2. Review Articles
  3. Mitochondrial thermogenesis in cancer cells
  4. Application of indocyanine green in the management of oral cancer: a literature review
  5. Long non-coding RNA, FOXP4-AS1, acts as a novel biomarker of cancers
  6. The role of synthetic peptides derived from bovine lactoferricin against breast cancer cell lines: a mini-review
  7. Single cell RNA sequencing – a valuable tool for cancer immunotherapy: a mini review
  8. Research Articles
  9. Global patterns and temporal trends in ovarian cancer morbidity, mortality, and burden from 1990 to 2019
  10. The association between NRF2 transcriptional gene dysregulation and IDH mutation in Grade 4 astrocytoma
  11. More than just a KRAS inhibitor: DCAI abrogates the self-renewal of pancreatic cancer stem cells in vitro
  12. DUSP1 promotes pancreatic cancer cell proliferation and invasion by upregulating nephronectin expression
  13. IMMT promotes hepatocellular carcinoma formation via PI3K/AKT/mTOR pathway
  14. MiR-100-5p transfected MSCs-derived exosomes can suppress NSCLC progression via PI3K-AKT-mTOR
  15. Inhibitory function of CDK12i combined with WEE1i on castration-resistant prostate cancer cells in vitro and in vivo
  16. Prognostic potential of m7G-associated lncRNA signature in predicting bladder cancer response to immunotherapy and chemotherapy
  17. Case Reports
  18. A rare FBXO25–SEPT14 fusion in a patient with chronic myeloid leukemia treatment to tyrosine kinase inhibitors: a case report
  19. Stage I duodenal adenocarcinoma cured by a short treatment cycle of pembrolizumab: a case report
  20. Rapid Communication
  21. ROMO1 – a potential immunohistochemical prognostic marker for cancer development
  22. Article Commentary
  23. A commentary: Role of MTA1: a novel modulator reprogramming mitochondrial glucose metabolism
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